What is the blood supply to hemorrhoids?

Blood Supply of Hemorrhoids

Hemorrhoids receive their arterial blood supply from the terminal branches of the superior rectal artery, which forms an arteriovenous plexus within the anal cushions, with significantly increased caliber and flow velocity in patients with hemorrhoidal disease compared to healthy individuals. 1

Arterial Supply

Internal hemorrhoids are supplied by terminal branches of the superior rectal artery (SRA), which arise from the inferior mesenteric artery. 1 These arterial branches form arteriovenous communications within the submucosal space of the anal cushions, creating the corpus cavernosum recti (CCR). 1

• In patients with hemorrhoids, the mean arterial caliber measures 1.87 ± 0.68 mm (range 0.6-3.60 mm), compared to only 0.92 ± 0.15 mm in healthy controls—a statistically significant difference. 1
• Arterial blood flow velocity is markedly elevated in hemorrhoidal disease, averaging 33.9 cm/second versus 11.9 cm/second in controls. 1
• This hypervascularization likely contributes to hemorrhoid growth rather than being a consequence of the disease. 1

External hemorrhoids originate from the inferior hemorrhoidal plexus below the dentate line. 2 These are distinct vascular structures covered by anoderm and highly innervated by somatic pain receptors. 2

Pathophysiologic Vascular Changes

The American Gastroenterological Association describes hemorrhoids as abnormal swelling of anal cushions with dilation of the submucosal arteriovenous plexus, though the exact pathogenesis remains incompletely understood. 3 The anal cushions are normal vascular structures consisting of connective tissue surrounding arteriovenous communications between terminal SRA branches and rectal veins. 3

• Abnormal dilatation and distortion of vascular channels, combined with destructive changes in supporting connective tissue, represents the paramount pathologic finding. 4
• Dysregulation of vascular tone and vascular hyperplasia appear to play important roles in hemorrhoid development. 4
• These vascular changes contribute 15-20% of resting anal pressure. 3

Clinical Distinction from Anorectal Varices

A critical pitfall is confusing hemorrhoids with anorectal varices, which have entirely different vascular origins and require different management. 5

Portal hypertension causes anorectal varices that are distinct from hemorrhoids and should not be considered a cause of hemorrhoids. 5 Patients with portal hypertension and varices do not have an increased incidence of hemorrhoids. 5

• Anorectal varices are discrete, compressible, serpiginous submucosal varicose veins that cross the dentate line and extend cranially into the rectum. 5
• Hemorrhoids are abnormal anal cushions with dilatation of the hemorrhoidal venous plexus confined within the anal canal. 5
• Standard hemorrhoidal treatments should never be used for variceal bleeding; instead, correction of underlying portal hypertension is required. 5

Therapeutic Implications

The arterial nature of hemorrhoidal blood supply has led to targeted interventions:

• Doppler-guided hemorrhoidal artery ligation targets the terminal branches of the superior rectal artery supplying the corpus cavernosum recti. 1
• Superior rectal artery embolization represents an emerging minimally invasive alternative to conventional surgical approaches. 6
• Rubber band ligation works by cutting off blood supply to hemorrhoidal tissue, leading to ischemia, necrosis, and eventual sloughing, with 89% symptom resolution. 7